P0905INFLUENCE OF TUMOR NECROSIS FACTOR ON MINERAL BONE DISEASE IN ESRD PATIENTS

Abstract

Abstract Background and Aims Serum levels of parathyreoid hormone is the main cause of mineral disorders in patients on chronic hemodialysis, and it well known that this hormone acts as an uremic toxine and contributes to oxidative stress and overall mortality rate. However, there are many observations which imply that the protean manifestations of renal bone disease cannot be explained simply by abnormalities of PTH or vitamin D metabolites. For example, levels of PTH correlate relatively poorly with various parameters of bone histology. It has been shown that uremia leads to cytokijne imbalance with overbalance of proinflammatory citokines such as TNF. Also, studies showed that calcimimetic therapy decreases not only PTH levels, but also levels of TNF. The aim was to analyse tumor necrosis factor (TNF) gene polymorphisms in group of hemodialysis patients and to correlate the findings with presence of secondary hyperparathyroidism. Method This cross sectional study included 202 patients on regular hemodialysis for more than six months in University Medical Centar Zvezdara. Venous blood for genotyping and for PTH analysis was collected on midweek dialysis session from each patient. Genetic analysis was performed by using polymerase chain reaction. Patients are diveded in two groups regarding the level of PTH, so that first group had normal PTH levels or mild SHPT, while patients in second group had sever SHPT. We analysed influence of genetic polymorphism for TNF on apperance of SHPT. Results The results have shown 3 fold lower risk for developing SHPT in GG homozygots for TNF gene with statistical significance (p=0,01)- Table 1. Conclusion Parathyreoid gland hyperfunction is multifactorial disorder and there are emerging evidence that cytokines as endogenous modulators have an important impact on its pathogenesis.